JACC Report 40 – Peracetic Acid and its Equilibrium Solutions

Abstract

JACC 040 : Peracetic Acid (CAS No. 79-21-0) and its Equilibrium Solutions | January 2001

This report has been produced as part of the Joint Assessment of Commodity Chemicals (JACC) programme. It presents a critical evaluation of the physicochemical, ecotoxicity and toxicity data of peracetic acid (PAA) solutions. At present no other comprehensive review is available. A risk assessment, inter alia, will be required under the EU Biocidal Products Directive (European Parliament and Council Directive 98/8/EC concerning the placing of biocidal products on the market). Most studies have been performed with different grades of equilibrium PAA solutions, i.e. formulations containing PAA, acetic acid and hydrogen peroxide dissolved in water in different concentration ratios. PAA solutions are clear, colourless and acidic liquids with a pungent vinegar-like odour. Upon dilution with water, their components tend to re-equilibrate slowly within several days. Solutions with a high (> 15%) PAA content can produce flammable vapours and exothermic decomposition can occur, liberating large volumes of oxygen gas. To guard against this, commercial PAA formulations are stabilised. If released into the environment PAA will be distributed almost entirely to the aquatic compartment, where it is degraded by hydrolysis or decomposition. Hydrolysis is faster at high pH, such as in seawater. Biodegradation is rapid, although limited by the biocidal effect of PAA at higher concentrations. Bioaccumulation is not expected to occur. PAA solutions are acutely toxic to aquatic organisms. The toxicity is related to the PAA content, except for solutions with a relatively high ratio of hydrogen peroxide. In those cases, the toxicity is attributable to the hydrogen peroxide. The studies of acute mammalian toxicity do not reveal a clear dose-response that could be related to the PAA content or concentration alone. A particular problem with the inhalation studies is the instability of the vapour/aerosol phase. The available repeated-dose toxicity studies suffer from deficiencies in reporting, inadequate histopathological examination and limited number of dose levels tested. The presence of infectious disease in a number of the animal studies obscured and confounded the test findings. It was thus not possible to derive clear, no-adverse effect levels from the existing studies. In spite of these limitations, it can be concluded that the main effect of PAA seen in experimental animals is severe irritation and corrosion of skin, eyes and mucous membranes. This is consistent with information on human exposure. However, the limited data available suggest that a systemic effect after repeated exposure to PAA cannot be completely excluded. The skin sensitisation potential of PAA appears to be low. The data do not raise immediate concern for mutagenicity, carcinogenicity or toxicity to reproduction.